The
Epidemiology of Alcoholic Liver Disease

Robert
E. Mann, Ph.D., is a senior scientist in the Department of Social, Prevention
and Health Policy Research at the Centre for Addiction and Mental Health
and an associate professor in the Department of Public Health Sciences
at the University of Toronto, both in Toronto, Canada.

Reginald
G. Smart, Ph.D., is a principal and senior scientist in the Department
of Social, Prevention and Health Policy Research at the Centre for Addiction
and Mental Health in Toronto, Canada.

Richard
Govoni, Ph.D., is a research fellow in the Department of Public Health
Sciences at the University of Toronto and an assistant professor in
the Department of Psychology at the University of Windsor in Windsor,
Canada.

The
preparation of this work was supported in part by a fellowship to R.
Govoni from the Ontario Problem Gambling Research Centre.

This article
describes the various forms of alcoholic liver disease (ALD), with particular
emphasis on cirrhosis, the form of liver disease that often is most associated
with alcohol abuse and about which the most information is available. Epidemiological
research has evaluated the prevalence of ALD and the factors that often contribute
to the disease. Although the most potent factor in ALD is the excessive consumption
of alcoholic beverages, gender and ethnic differences also account for some
important variations in rates of liver disease. Mortality rates from cirrhosis
have declined in the United States and some other countries since the 1970s.
A number of factors may have contributed to this decline, including increased
participation in treatment for alcohol problems and Alcoholics Anonymous membership,
decreases in alcohol consumption, and changes in the consumption of certain
types of alcoholic beverages.
Key words: alcoholic liver cirrhosis; epidemiological indicators; gender differences;
ethnic differences; AODR (alcohol and other drug related) mortality; morbidity;
AOD (alcohol and other drug) use pattern; risk factors; trend; aggregate AOD
consumption; beneficial vs adverse drug effect; Alcoholics Anonymous; United
States; survey of research

One of the most enduring
insights into the effects of alcohol has been the assertion that heavy alcohol
consumption increases mortality rates, especially those from cirrhosis of
the liver and other forms of liver disease (see the sidebar, below). The scientific
study of alcohol–related mortality began in the 1920s with Pearl’s
studies (1926) of death rates among various types of drinkers. He and others
found that heavy drinkers had higher rates of overall mortality and of mortality
from cirrhosis than did lighter drinkers or abstainers. Since then, mortality
studies have continued to demonstrate that heavy drinkers and alcoholics die
from cirrhosis at a much higher rate than the general population (Mann et
al. 1993; Pell and D’Alonzo 1973; Schmidt and de Lint 1972; Thun et
al. 1997). In addition, laboratory studies conducted in the 1930s established
that feeding large amounts of alcohol to rats and other animals caused liver
disease (Lelbach 1974).

SIDEBAR

Types of Alcoholic
Liver Disease

The most prevalent
types of alcoholic liver disease are fatty liver, alcoholic hepatitis,
and cirrhosis. Often, as people continue to drink heavily, they progress
from fatty liver to hepatitis to cirrhosis. The disorders can also occur
together, however, and liver biopsies can show signs of all three in
some people (Kirsh et al. 1995).

Alcoholic
Fatty Liver

About 20 percent
of alcoholics and heavy drinkers develop fatty liver, or steatosis.
In many cases there are no clinical symptoms except for an enlarged
liver (hepatomegaly). Fatty liver can be reversed if alcohol consumption
is stopped or significantly reduced, but the condition can lead to death
if alcohol consumption is not reduced or stopped. Some biopsies from
people with fatty liver show inflammatory changes, an early sign of
more serious liver disease.

Alcoholic
Hepatitis

Alcoholic hepatitis
usually is diagnosed when a liver biopsy indicates inflammatory changes,
liver degeneration, fibrosis, and other changes to liver cells. Common
clinical signs of alcoholic hepatitis include swollen liver, nausea,
vomiting, and abdominal pain. Patients also may experience fever, jaundice,
liver failure, and bleeding. The rate of mortality in severe cases is
about 50 percent. If heavy drinking continues, about 40 percent of cases
of alcoholic hepatitis will develop into cirrhosis.

Alcoholic
Cirrhosis

Cirrhosis of the
liver is the most serious form of ALD and a cause of many deaths and
serious illnesses. In cirrhosis, scar tissue replaces normal liver tissue,
disrupting blood flow through the liver and preventing it from working
properly. Clinical signs of cirrhosis include redness of the palms caused
by capillary dilation (palmar erythema); shortening of muscles in the
fingers (contractures) caused by toxic effects or fibrous changes; white
nails; thickening and widening of the fingers and nails (clubbing);
liver enlargement or inflammation; and abnormal accumulation of fat
in normal liver cells (fatty infiltration). Diagnosis of cirrhosis must
be made with biopsies, although laboratory tests can be helpful as well.

About 10 percent
to 15 percent of people with alcoholism develop cirrhosis, but many
survive it. Many are unaware that they have it, and about 30 percent
to 40 percent of cirrhosis cases are discovered at autopsy (Anand 1999).
The 5–year survival rate for people with cirrhosis who stop drinking
is about 90 percent, compared with 70 percent

of those who do
not stop drinking. However, for late–stage cirrhosis—that
is, when jaundice, accumulation of fluid in the abdomen (ascites), or
gastrointestinal bleeding have occurred—the survival rate is only
60 percent for those who stop drinking and 35 percent for those who
do not.

Other
Forms of Liver Disease Affected by Alcohol

Alcohol can be a
factor in other forms of liver disease not specifically attributed to
it, and alcohol may interact with risk factors for other forms of liver
disease. For example, people with alcohol–related cirrhosis are
at much higher risk for the development of liver cancer (Hall 1995).
Likewise, heavy drinking in combination with hepatitis B or C substantially
increases the risk of liver cirrhosis, compared with the risk associated
with heavy drinking alone (Corrao et al. 1998).

—Robert
E. Mann, Reginald G. Smart, and Richard Govoni

References

Anand, B.S. Cirrhosis
of the liver. Western Journal of Medicine 171: 110–115,
1999.

Alcohol consumption increased
substantially in many countries after World War II, which spurred greater
interest in the effects of alcohol consumption on cirrhosis and other forms
of alcoholic liver disease (ALD). One of the most influential efforts to summarize
research in this area was undertaken in 1975 by an international group of
scientists sponsored by the World Health Organization (WHO). The resulting
book, Alcohol Control Policies in Public Health Perspective (Bruun
et al. 1975), reviewed studies of clinical and nonclinical populations of
heavy drinkers. All studies found that a greater proportion of heavy drinkers
died of cirrhosis than would be expected based on rates of cirrhosis deaths
in the general population (i.e., liver cirrhosis deaths among heavy drinkers
ranged from 2 to 23 times higher than the rate that would be expected in the
general population). This research established a firm connection between heavy
alcohol consumption and liver disease. Investigators also have observed that
the price of alcohol is a significant determinant of alcohol consumption and
thus of cirrhosis mortality rates (Bruun et al. 1975; Edwards et al. 1994;
Seeley 1960). These findings have laid the foundation for an influential public
health approach to controlling liver disease and other alcohol problems that
emphasizes the control of alcohol’s availability and includes recommendations
to control cirrhosis and other alcohol–related problems through taxation
(Chaloupka et al. 2002; Cook and Tauchen 1982). The validity of this availability–control
approach has been widely supported (e.g., Edwards et al. 1994), and investigations
of the epidemiology of ALD have continued to be central to it (e.g., Ramstedt
2001).

Drinking Patterns and
Alcoholic Liver Disease

Many studies show that
the amount of alcohol consumed and the duration of that consumption are closely
associated with cirrhosis.1 (1 In examining trends in
alcoholic liver disease, some authors have considered only those cases directly
attributable to alcohol [e.g., Douds et al. 2003]. Other authors have determined
that many cirrhosis deaths coded as not involving alcohol are in fact alcohol
related [particularly for some age groups, including the middle–aged];
thus, these authors have examined total cirrhosis deaths when evaluating trends
[e.g., Ramstedt 2001].) One of the best demonstrations of this association
was presented by Lelbach (1974), who studied 319 patients in an alcoholism
clinic in Germany. He calculated the average amount of alcohol consumed per
hour in a 24–hour day. As shown in table 1, patients with normal liver
function consumed far less alcohol than did those with cirrhosis. Those who
did not have cirrhosis but did have other liver malfunctions had intermediate
rates of alcohol intake. In addition, patients with normal liver function
had been drinking heavily for only about 8 years on average, whereas those
with cirrhosis had been drinking heavily for more than 17 years on average.
As this research illustrates, the risk of developing cirrhosis is a function
of both quantity and duration of alcohol consumption. Bellentani and Tiribelli
(2001) recently proposed that cirrhosis does not develop below a lifetime
alcohol ingestion of 100 kg of undiluted alcohol. This amount corresponds
to an average daily intake of 30 grams of alcohol (between two and three drinks2
[2 The National Institute on Alcohol Abuse and Alcoholism
(NIAAA) defines a standard drink as 11–14 grams (g) of alcohol, which
corresponds to approximately one shot of 80–proof alcohol (about 14
g alcohol), one glass of wine (11 g), or one 12–oz beer (12.8 g).])
for 10 years. These investigators also noted that consuming alcohol with food
resulted in somewhat lower levels of risk than consuming alcohol by itself.

NOTES: Patients with normal
liver function consumed far less alcohol and had been drinking for fewer years
than those with cirrhosis. Those who did not have cirrhosis but did have other
liver malfunctions had intermediate rates of alcohol intake. See sidebar,
p. 211, for definitions of alcoholic liver disease.

SOURCE: Adapted from Lelbach
1974.

More recent studies confirm
the close association between alcohol consumption and cirrhosis risk. Anderson
(1995) examined data from four case control studies in men and women. (Figure
1 shows results from representative studies [Coates et al. 1986, and Tuyns
and Péquignot 1984].) This investigation showed that the risk of cirrhosis
was related to the amount of alcohol consumption in every study. In addition,
as alcohol consumption increased, the risk of cirrhosis increased more rapidly
for females than it did for males. The link between gender and risk for cirrhosis
is addressed in detail in the section on page 215.

Figure
1 Alcohol
consumption and incidence of cirrhosis of the liver in men (m) and women
(w). Studies have shown a close relationship between alcohol consumption
and cirrhosis risk.

Note: Data truncated
at 70 g/day.

Cirrhosis Morbidity and
Mortality and Average Alcohol Consumption

The strong link between
heavy or excessive alcohol use and the development of liver disease took on
added significance in the middle of the 20th century, when several researchers
began exploring cirrhosis as a potential marker for levels of alcohol problems
in populations (Jellinek and Keller 1952; Ledermann 1956; Seeley 1960; Terris
1967). Of particular importance was the discovery of a relationship between
cirrhosis mortality rates and per capita levels of alcohol consumption in
the population. This relationship has proved to be remarkably strong and has
been consistently observed across time periods and in various regions of the
world (Bruun et al. 1975; Ramstedt 2001; Smart and Mann 1991). European researchers
have observed a lagged relationship between cirrhosis mortality and consumption
measures, with the rate of cirrhosis mortality in a year being influenced
by the alcohol consumption rates of several previous years (Corrao 1998; Ramstedt
2001). To account for this effect, Skog (1980) developed a “distributed
lag model,” in which the effects of alcohol consumption in a year are
distributed over the next several years. Using this model, he was able to
explain an apparent inverse relationship between consumption and cirrhosis
mortality rates in Great Britain between 1931 and 1958 (Popham 1970). Incorporating
the distributed lag model into the data produced the expected positive relationship
between consumption and cirrhosis mortality.

Trends in Cirrhosis Mortality
Rates

Liver cirrhosis is a major
cause of death in the United States (Yoon et al. 2002; Minino et al. 2002).
In 2000, it was the 12th leading cause of death, accounting for 1.1 percent
of all deaths, with an age–adjusted death rate3 of 9.6 per
100,000 population. (3 Age adjustment is a statistical method of
adjusting for age differences, between populations or over time, that might
otherwise distort mortality trends. In the case of chronic diseases, including
cirrhosis of the liver, unadjusted mortality rates may appear to be higher
for older populations than for younger populations because mortality rates
are higher, on average, in older people.) Cirrhosis mortality rates vary substantially
among age groups: They are very low among the young but increase considerably
in middle age, reaching a peak of 31.1 per 100,000 among people ages 75 to
84. Because of the increase in cirrhosis mortality rates in middle age, the
contribution of cirrhosis to total deaths reaches a peak in the 45–54
age group, for which it is the fourth leading cause of death. In relation
to the cirrhosis mortality rate in other countries, the United States is in
the middle range, as are countries such as Belgium and Canada (WHO 2000).
Higher rates are seen in countries where people traditionally consume more
alcohol than in the United States, such as Spain, France, and Italy. In countries
where alcohol consumption is traditionally lower—Iceland, New Zealand,
and Norway, for example—cirrhosis death rates are lower.

Cirrhosis mortality rates
in the United States have changed substantially over time. Early in the 20th
century, these rates were at their highest point. As shown in figure 2, overall
cirrhosis mortality rates declined precipitously with the introduction of
Prohibition. When Prohibition ended, alcohol consumption and cirrhosis mortality
rates increased until the late 1960s and early 1970s, when these rates began
to approach levels seen in the first decade of the century. However, in the
mid–1970s cirrhosis mortality rates began to decline as they had with
the introduction of Prohibition; cirrhosis was the 8th leading cause of death
in 1977 (Galambos 1985) but the 12th leading cause of death by 2000. Similar
declines in cirrhosis mortality rates have been observed in many developed
countries (including Canada, Sweden, France, and Italy), but in other developed
countries (e.g., Great Britain, Finland, Denmark) cirrhosis death rates have
increased (Ramstedt 2001). The reasons for the dramatic reductions remain
a source of considerable interest, as will be discussed below.

Cirrhosis mortality rates
may continue to decline if alcohol consumption rates remain low or fall further.
However, the increase in cases of hepatitis C infection in the United States,
which are predicted to peak by 2015 (Armstrong et al. 2000), may affect the
rate of cirrhosis deaths. Because people infected with hepatitis C are more
likely to develop cirrhosis when they drink, death rates from cirrhosis may
increase in the future, even if drinking levels decline. (For more information
on hepatitis C infection and alcohol, see the article by Schiff and Ozden
in this issue.)

Reasons for Decreases
in Cirrhosis Death Rates

Changes in
Per Capita Alcohol Consumption

Changes in per capita
consumption of alcohol must be considered a leading candidate for the cause
of recent reductions in cirrhosis mortality rates. Research demonstrates that,
over a long period, changes in per capita consumption are broadly consistent
with changes in cirrhosis mortality rates (Ramstedt 2001; Singh and Hoyert
2000; Xie et al. 2000) (see figure 2). However, cirrhosis mortality in the
United States, Canada, and some other regions began to decline in the mid–1970s,
before per capita consumption rates began to go down (also see figure 2).
This is the opposite of what would be expected based on the hypothesized lagged
relationship between per capita consumption and cirrhosis mortality rates.
Thus, researchers are considering whether other factors also have influenced
cirrhosis mortality rates in recent years.

Beverage–Specific
Effects

The relationship between
cirrhosis mortality and alcohol consumption may vary depending on the type
of alcoholic beverage—beer, wine, or spirits—consumed. Any such
beverage–specific effects could help explain why cirrhosis mortality
began to decline in the 1970s despite the continued rise in total alcohol
consumption.

Researchers over the past
four decades have investigated this question (e.g., Terris 1967; Gruenewald
and Ponicki 1995; Schmidt and Bronetto 1962). Recently, Roizen and colleagues
(1999) and Kerr and colleagues (2000) have proposed that cirrhosis mortality
is more strongly associated with consumption of spirits than with other alcoholic
beverages, and that this relationship accounts for the apparent discrepancy
between per capita alcohol consumption measures and cirrhosis mortality rates.
Roizen and colleagues (1999) examined U.S. cirrhosis mortality data from 1949
to 1994 and observed that consumption of spirits was more strongly related
to cirrhosis mortality than was total alcohol consumption, a finding that
is consistent with earlier observations of U.S. data (Terris 1967). Kerr and
colleagues (2000) extended this analysis to several other countries, with
similar results. The relationship between spirits consumption and cirrhosis
mortality during the 1970s, when cirrhosis mortality rates began to decline
in the United States, suggests that the discrepancy between cirrhosis rates
and per capita alcohol consumption observed at that time arose because research
did not focus on spirits, the beverage most strongly related to cirrhosis
mortality.

The stronger association
between cirrhosis mortality and consumption of spirits may be attributable
to biological and sociobehavioral mechanisms. Some types of alcoholic beverage
may be more toxic to the liver than others (Lelbach 1974; Schmidt and Bronetto
1962). In addition, consumption of certain alcoholic beverages may be associated
with different drinking styles (Smart 1996)—that is, people who tend
to drink frequently and heavily, and thus are at greatest risk for developing
cirrhosis, also may tend to drink spirits rather than beer or wine. Thus,
drinking style may collude with biological mechanisms to significantly raise
some drinkers’ risk of liver disease. This interesting and important
issue is the subject of ongoing investigation.

Another possible reason
for declines in cirrhosis mortality has been increased participation in treatment
for alcohol abuse and in Alcoholics Anonymous meetings (Mann et al. 1988a,
b; Holder and Parker 1992; Romelsjš 1987; Smart and Mann 2000). Specifically,
cirrhosis morbidity and mortality rates could be influenced if participation
in alcoholism treatment and AA are in some degree effective in reducing excessive
drinking among heavy or abusive drinkers, if sufficient treatment occurs,
and if enough alcoholics become members of AA or receive other treatment services.
The 1970s and 1980s saw large increases in AA participation and in the number
of people who received alcoholism treatment services (Mann et al. 1988b,
1991). Smart and Mann (1993) examined whether these increases in treatment
and AA participation could affect cirrhosis morbidity and mortality rates.
According to estimates derived from the research:

Alcoholics seeking
treatment drink an average of 160 g of undiluted alcohol per day.

About 14 percent
of alcoholics will develop cirrhosis if they drink this quantity for a
period of 8 years.

About 50 percent
of alcoholics receiving treatment or attending AA meetings improve sufficiently
to postpone the development of cirrhosis or avoid death if they already
have cirrhosis.

The authors applied these
figures to the actual number of people who were AA members or were receiving
alcohol abuse treatment in 1975 and 1986 in Ontario and the United States.
Based on this analysis, between 25 percent and 100 percent of the actual reduction
in cirrhosis deaths and hospital discharges during the period could be predicted,
depending on the degree of overlap between treatment and AA membership that
was assumed.

Other studies of the relationship
between cirrhosis mortality rates and aggregate, or population, levels of
treatment and AA membership rates support the hypothesis that increases in
treatment and AA membership helped reduce cirrhosis mortality rates, both
in the United States and elsewhere. Several studies (for a review, see Smart
and Mann 2000) have found an association between reductions in cirrhosis morbidity
and mortality and increased levels of treatment and AA membership in Canada
(Mann et al. 1988b), the United States (Mann et al. 1991), and Sweden
(Leifman and Romelsjš 1997; Romelsjš 1987). Examining monthly cirrhosis mortality
data from North Carolina, Holder and Parker (1992) found that alcohol abuse
treatment had a significant short–term lagged relationship with cirrhosis
mortality, with an increase in treatment being followed 3 months later by
a decline in cirrhosis mortality. Finally, Smart and colleagues (1996) found
that increased funding for alcoholism treatment was associated with cirrhosis
mortality reductions across the United States. Thus, the data so far provide
strong support for the proposition that if a large enough portion of the population
participates, AA membership and alcohol abuse treatment can influence cirrhosis
morbidity and mortality rates at the population level.

Other Factors Associated
With Increased Rates of Cirrhosis Morbidity and Mortality

Gender Differences

As discussed above, historically
the epidemiology of cirrhosis has been linked closely to types and patterns
of alcohol consumption. Other factors also may be at work in the development
of liver disease. For example, there are important and long–standing
gender differences in cirrhosis mortality risk and mortality rates. As shown
in figure 2, cirrhosis mortality rates are about two times higher in men than
in women. These rates reflect the fact that men typically drink more than
women, and that the proportion of heavy drinkers and alcoholics is much higher
among men. However, as noted previously, it also appears that at any given
level of alcohol consumption, women have a higher likelihood of developing
cirrhosis than men (see figure 1) (Tuyns and Péquignot 1984). This phenomenon
is poorly understood, but several possible explanations have been offered.
One is that levels of alcohol dehydrogenase, an enzyme involved in breaking
down alcohol, may be lower in the stomachs of females than in males, which
would result in a higher blood alcohol content for females than for males
who consume equivalent amounts of alcohol (Frezza et al. 1990). Because damage
to the liver is a function of blood alcohol levels and exposure time, factors
that lead to higher blood alcohol concentrations could at least partially
explain females’ higher risk for alcohol–related cirrhosis. Another
possible explanation is that estrogen may increase the susceptibility of the
liver to alcohol–related damage (Ikejima et al. 1998; Colantoni et al.
2003). Behavioral factors, including drinking patterns and diet, also may
contribute to females’ higher cirrhosis risk.

Figure
2 Age–adjusted
death rates of liver cirrhosis by gender, 1910–1932 in death registration
States, and 1933–1997 in entire United States. U.S. cirrhosis
mortality rates were high at the beginning of the 20th century, declined
precipitously with the introduction of Prohibition, and increased again
when Prohibition ended. Mortality rates continued to increase until
the early to mid–1970s, when these rates began to approach the
levels seen in the first decade of the century. In the mid–1970s
cirrhosis mortality rates began to decline again, as they had with the
introduction of Prohibition, and they have continued to decline.

INSET (shaded area):
Per capita alcohol consumption for the years 1935 to 1999, illustrating
the link between alcohol consumption and cirrhosis mortality.

Genetic factors, including
those that influence alcohol metabolism and risk for alcoholism, also may
be involved in the increased risk for cirrhosis seen in women (Reed et al.
1996), but there still is considerable debate on this issue, and further research
is needed on the nature and the extent
of such genetic contributions.

In a recent study, Corrao
and colleagues (1998) found that 98.1 percent of cirrhosis cases in men but
only 67.0 percent of cases in women could be attributed to alcohol consumption,
hepatitis C, and hepatitis B. The risk factors for cirrhosis appear to be
more complex for women than they are for men, and more research will be required
to identify and understand them.

Ethnic Differences

Important differences
in cirrhosis rates and cirrhosis mortality also exist among ethnic groups.
Although ethnic group differences have been declining in recent years, cirrhosis
rates remain higher for Blacks than for Whites in the United States (see figure
3), and the highest cirrhosis mortality rates currently are observed among
Hispanic groups (Stinson et al. 2001). Although these differences in cirrhosis
rates among Blacks, Whites, and Hispanics seem to suggest higher alcohol consumption
levels among Hispanics and Blacks than among Whites, studies of alcohol consumption
patterns in these groups tend not to support this interpretation. For example,
in recent years, alcohol consumption among Blacks has been less than or comparable
with that of Whites (see table 2).

Figure
3 Age–adjusted
rates of alcohol–related cirrhosis by gender and ethnic group
(Black, White, and Hispanic), United States, 1970–1998.

SOURCE: Yoon et
al. 2001. (Categories shown in this figure were those used in the source
study.)

Table 2 Consumption
Patterns for Blacks and Whites, 1984 and 1992

Consumption
Level

1984

1992

Blacks (%)

Whites (%)

Blacks (%)

Whites (%)

Males

Abstainer

29

23

35

28

Infrequent

13

13

6

9

Less frequent

12

16

19

21

Frequent

30

27

25

29

Frequent
heavy

16

19

15

12

Females

Abstainer

46

31

51

36

Infrequent

18

23

24

22

Less frequent

19

19

12

24

Frequent

13

23

8

15

Frequent
heavy

4

4

5

3

NOTES: In recent years,
alcohol consumption among Blacks has been comparable to or less than that
of Whites.
Some columns do not total 100 percent because of rounding.

SOURCE: Adapted from Jones–Webb
1998.

Several reasons for ethnic
group differences in cirrhosis rates have been proposed, including demographic
factors related to gender, age, income, education, and employment; biological
factors, such as family history of drinking problems; and environmental factors,
such as stress (for a review, see Jones–Webb 1998). Other suggested
factors are differential access to alcoholism treatment services (Singh and
Hoyert 2000), although as yet no data are available to support this explanation;
and differing rates of hepatitis C infection, which appears to be more prevalent
among Hispanics than in Black and White populations (Yen et al. 2003). Ethnic
group differences in cirrhosis risk and mortality may be linked to the possibility
that, over time, general health status has improved more for some ethnic groups
than others. However, as summarized in table 3, two general health indicators—age–adjusted
death rate and life expectancy at birth—showed comparable gains for
Blacks and Whites between 1970 and 2000. Thus, it is not yet possible to attribute
changes in cirrhosis rates to changes in general health indicators of various
groups.

Table 3 General
Health Indicators for U.S. Blacks and Whites, 1970 and 2000

Black Males

White Males

Black Females

White Females

Age–Adjusted
Death Rate per 100,000 Population*

1970

1,873.9

1,513.7

1,228.7

1,193.3

2000

1,377.8

1,018.2

947.9

739.1

Percent change

–26.5

–32.7

–22.9

–30.1

Life
Expectancy (years)

1970

60.0

68.0

68.3

75.6

2000

68.2

74.8

74.9

80.0

Percent change

+13.7

+10.0

+9.7

+5.8

*Standardized to 2000
age distribution.

NOTE: Between 1970 and
2000, Blacks and Whites showed comparable gains in age–adjusted death
rate and life expectancy at birth.

SOURCE: Minino et al.
2002.

As this discussion indicates,
cirrhosis rates in subpopulations, such as those based on gender or ethnicity,
can show significant deviations from the rates of cirrhosis that would be
expected from alcohol consumption levels alone. These differences, which are
not yet well understood, have important implications for research and prevention
initiatives. From a public health perspective, an understanding of subpopulation
dynamics is critical to the development of programs for preventing alcoholic
liver disease.

Conclusion

Alcoholic liver disease
is a major source of alcohol–related morbidity and mortality. Heavy
drinkers and alcoholics may progress from fatty liver to alcoholic hepatitis
to cirrhosis, and it is estimated that 10 percent to 15 percent of alcoholics
will develop cirrhosis. The likelihood of developing ALD is, to a large extent,
a function of both the duration and amount of heavy drinking, and the per
capita consumption of alcohol within populations has been shown to be a strong
determinant of cirrhosis mortality rates. Recent studies also suggest that
alcohol and hepatitis C may exert a multiplicative effect on risk for cirrhosis
and other liver disease.

Although ALD remains a
major cause of death, important declines in ALD death rates have been observed
in recent years. Undoubtedly these declines were caused in part by changes
in alcohol consumption rates, but because the mortality rate decline began
when consumption was still increasing, other factors appear to be involved
as well. To date, the evidence indicates that increases in participation in
AA and other treatment for alcohol abuse have played an important role in
reducing cirrhosis mortality rates. Other research has suggested that cirrhosis
mortality rates may be more closely related to consumption of certain alcoholic
beverages—specifically spirits—than to total alcohol consumption,
and that beverage–specific effects can account for the fact that cirrhosis
rates appeared to decrease although consumption rates were increasing in the
1970s. Important differences in ALD rates in men and women and among different
ethnic groups have been found as well.

Further research into
these differences is likely to lead to improved prevention and treatment of
alcohol–related liver disease.

Mann, R.E.; Smart, R.G.;
Anglin, L.; and Rush, B. Are decreases in liver cirrhosis rates a result of
increased treatment for alcoholism? British Journal of Addiction
83:683–688, 1988b.

Mann, R.E.; Smart, R.G.;
Anglin, L.; and Adlaf, E. Reductions in cirrhosis in the United States: Associations
with per capita consumption and AA membership. Journal of Studies on Alcohol
52:361–365, 1991.

Ode to the Liver

Modest,
organized
friend,
underground
worker,
let me give you
the wing of my song,
the thrust
of the air,
the soaring
of my ode:
it is born
of your invisible
machinery,
it flies
from your tireless
confined mill,
delicate
powerful
entrail,
ever alive and dark.

While
the heart resounds and attracts
the music of the mandolin,
there, inside,
you filter
and apportion,
you separate
and divide,
you multiply
and lubricate,
you raise
and gather
the threads and the grams
of life, the final
distillate,
the intimate essences.

Submerged
viscus,
measurer
of the blood,
you live
full of hands
and full of eyes,
measuring and transferring
in your hidden
alchemical
chamber.

Yellow
is the matrix
of your red hydraulic flow,
diver
of the most perilous
depths of man,
there forever hidden,
everlasting,
in the factory,
noiseless.

And every feeling
or impulse
grew in your machinery,
received some drop
of your tireless
elaboration,
to love you added
fire or melancholy,
let one tiny cell
be in error
or one fiber be worn
in your labor
and the pilot flies into the wrong sky,
the tenor collapses in a wheeze,
the astronomer loses a planet.

Up above, how
the bewitching eyes of the rose
and the lips
of the matinal carnation
sparkle!

How the maiden
in the river laughs!

And down below,
the filter and the balance,
the delicate chemistry
of the liver,
the storehouse
of the subtle changes:
no one
sees or celebrates it,
but, when it ages
or its mortar wastes away,
the eyes of the rose are gone,
the teeth of the carnation wilted
and the maiden silent in the river.

Austere portion
or the whole
of myself,
grandfather
of the heart,
generator
of energy:
I sing to you
and I fear you
as though you were judge,
meter,
implacable indicator,
and if I can not
surrender myself in shackles to austerity,
if the surfeit of
delicacies,
or the hereditary wine of my country
dared
to disturb my health
or the equilibrium of my poetry,
from you,
dark monarch,
giver of syrups and of poisons,
regulator of salts,
from you I hope for justice:
I love life: Do not betray me! Work on!